| Abstract|| |
We describe postoperative refractory ventricular tachycardia (VT) in a patient following aortic and mitral valve replacement. Following an uneventful separation from cardiopulmonary bypass with dobutamine, the patient developed recurrent VT, 4 hours into the postoperative period. The VT did not respond to standard doses of xylocard, magnesium and amiodarone. Electrolyte and acid base parameters were normal. Multiple cardioversions failed to revert back to a stable rhythm. Intra-aortic balloon pumping was instituted and overdrive right ventricular pacing was unsuccessful. Following intravenous sotalol 80 mg, the VT came under control and reverted to a nodal rhythm, which required atrial pacing for the next 8 hours. Oral sotalol therapy was continued at 40 mg daily. The VT did not recur.
Keywords: Amiodarone; Cardioversion; Double valve replacement; Refractory ventricular tachycardia; Sotalol
|How to cite this article:|
Kandasamy A, Arumugham S, Krupanandha H, Reddy B. Sotalol: A rescue drug in the face of life-threatening refractory ventricular tachycardia. Ann Card Anaesth 2014;17:170-2
|How to cite this URL:|
Kandasamy A, Arumugham S, Krupanandha H, Reddy B. Sotalol: A rescue drug in the face of life-threatening refractory ventricular tachycardia. Ann Card Anaesth [serial online] 2014 [cited 2023 Jan 29];17:170-2. Available from: https://www.annals.in/text.asp?2014/17/2/170/129885
| Introduction|| |
Recurrent sustained ventricular arrhythmias after cardiac surgery are uncommon with reported incidences ranging from 0.41% to 1.4%.  The ventricular arrhythmias are potentially lethal and warrants immediate and aggressive treatment. Lidocaine appears to be effective in converting no more than 20% of ventricular tachycardia (VT).  Amiodarone is effective in the acute treatment of life-threatening VT that is resistant to lidocaine and cardioversion.  Failure of medical therapy with amiodarone requires prompt initiation of electrical therapy with direct current (DC) cardioversion or mechanical assist device. However, if the VT remains refractory in spite of all the above measures modalities, what one should do is not well described. We describe a case of recurrent VT, refractory to multiple drug treatment, cardioversion and mechanical assist device, which was terminated only after the administration the VT of intravenous sotalol.
| Case Report|| |
A 36-year-old man weighing 53 kg underwent double valve replacement for rheumatic valvular heart disease. Preoperative electrocardiography (ECG) showed right bundle branch block. Chest X-ray showed cardiomegaly. Transthoracic echocardiography (TTE) revealed moderate mitral and aortic stenosis, moderate mitral and aortic regurgitation, moderate pulmonary hypertension and an ejection fraction (EF) of 55%. Laboratory investigations were within normal limits. Patient was receiving oral digoxin, diuretics, amiodarone and penicillin prophylaxis. Oral diazepam 7.5 mg, pantoprazole 40 mg and intramuscular morphine 10 mg were given as premedication. Anesthetic induction was performed with fentanyl 6 μg/kg, midazolam 0.06 mg/kg and sevoflurane 1.5% and was maintained with fentanyl 2 μg/kg/h, midazolam 0.02 mg/kg/h and 0.8% sevoflurane. Vecuronium was administered to facilitate endotracheal intubation. Peak airway pressures after intubation was 20 cmH 2 O and EtCO 2 was 30-35 mmHg. Heart rate, invasive blood pressure and SpO 2 (100%) were within acceptable limits.
After conventional midline sternotomy and usual preparations, heparin 210 mg was administered and after achieving activated clotting time above 500 seconds, standard cardiopulmonary bypass (CPB) was initiated. Patient was cooled to 30°C. Adenosine 6 mg was administered immediately after application of aortic cross clamp (ACC), followed by hypothermic (10°C) hyperkalemic blood cardioplegia (CP). The cold blood CP was repeated every 15 min for myocardial protection. A retrograde coronary sinus cannula was also used for the intermittent delivery of CP. Heart was vented by using a right superior pulmonary vein vent. Mean perfusion pressure during CPB was maintained around 50 mmHg. Magnesium 3 g was administered on bypass. The aortic and mitral valves were replaced using 19 mm and 27 mm St. Jude mechanical prosthesis. The ACC and CPB times were 110 and 140 min, respectively. After rewarming, weaning from bypass was achieved with elective infusions of dobutamine 5 μg/kg/min and nitroglycerine 0.6 μg/kg/min without difficulty. Atrial pacing was started electively to increase the heart rate to 100/min. The arterial blood pressure (ABP) and the central venous pressure (CVP) were 92/50 and 6 mmHg, respectively.
Immediate postoperative ECG showed no evidence of myocardial ischemia. On blood gas analysis, serum potassium was 4.6 mEq/L and there was no evidence of acidosis. After an uneventful 4 h, the patient developed ventricular bigeminy followed by pulsatile VT. The ventricular rate was more than 190/min, the ABP was 82/46 mmHg and CVP was 10 mmHg. After two doses of lidocaine 2 mg/kg, amiodarone 150 mg was administered over 15 min, followed by amiodarone infusion 300 mg over 1 h. Potassium 15 mEq and magnesium 2 g were administered over 1 h. Amiodarone 1 mg/min and lidocaine 60 mg/h were started in view of sustained pulsatile VT. Blood gases, electrolytes, and blood sugar were within normal limits. Cardioversion was unsuccessful. The TTE revealed normally functioning prosthetic valves, no evidence of tamponade and EF of 30%. From the sixth postoperative hour, hypotension ensued (ABP <70 mmHg) with a CVP of 10 mmHg. Intra-aortic balloon pumping (IABP) was instituted. Mechanical causes of ventricular irritability like central venous catheter and mediastinal drain position were ruled out. Multiple shocks (>30) with chest compressions were performed as the patient had pulseless VT. Standard advanced cardiovascular life support protocols were followed. Right ventricular overdrive pacing was tried, but in vain. When all these therapies failed, sotalol was administered as a desperate measure. Following intravenous sotalol 80 mg, administered at a rate of 10 mg/min, the ventricular rate decreased from 190 to 124 beats/min. Subsequently, VT reverted to nodal rhythm with a rate of 46/min with a blood pressure of 70/46 mmHg. Atrial pacing was started at a rate of 100/min, which was required for the next 8 h. Levosimendan and noradrenaline were started at 0.06 μg/kg/min and 0.04 μg/kg/min. Intravenous sotalol 40 mg was repeated 8 hours after the first dose. The patient was arrhythmia free on the first postoperative day after which he was weaned off ventilator and IABP. Oral sotalol therapy was continued at 40 mg daily. Serial ECGs were taken for the next four days and there was no prolongation of QT interval. The VT did not recur. TTE after weaning from ventilator revealed an EF of 41%. Patient was discharged on the 10 th postoperative day with oral amiodarone, sotalol, acitrom, and furosemide.
| Discussion|| |
VT is a life-threatening arrhythmia, particularly when it results in hemodynamic compromise. The clinical situations associated with ventricular arrhythmias after cardiac surgery include electrolyte abnormalities, hypoxia, hypovolemia, myocardial ischemia, coronary air embolism, ischemia-reperfusion injury and proarrhythmia caused by inotropes. The standard management is the administration of antiarrhythmic drugs and electrical cardioversion. Amiodarone, a Class III antiarrhythmic agent, is the drug of choice in VT.  Failure of medical therapy requires electrical DC cardioversion. However, if a stable rhythm is not restored, other available resources are limited. Sotalol has been shown to suppress and prevent the reinduction of VT in patients with recurrent life-threatening VT.  It is a racemic compound with Class II (beta-blockade) and Class III (prolonged action potential) antiarrhythmic activity. It has been shown to increase the duration of action potentials and refractory periods throughout myocardial tissue and accessory pathways. The effect of sotalol on left ventricular function remains unclear. Lengthening the action potential duration may increase contractility, which may offset the depressant action of beta-adrenergic receptor antagonism. Unlike amiodarone, sotalol does not elevate and, indeed, may lower defibrillation threshold.  There is a small risk of proarrhythmia, specifically, torsade de pointes (2.5%). The majority of episodes of torsades de pointes occur with higher doses (>320 mg daily) and within 3 days of commencing sotalol therapy.  Prolongation of the QT interval >0.5 sec should be avoided.
This case report suggests that sotalol can be effectively used in patients with drug refractory VT. Before initiating sotalol therapy, pacing and defibrillation equipments should be readily available. Although the incidence of side-effects is high, patients appear to tolerate sotalol therapy well. 
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